Impacts of CO2 on acid-base balance, rectal base excretion and intestinal carbonate formation in marine fish

化石燃料的燃烧继续增加海洋中的二氧化碳（CO2），导致海洋酸化。此外，在某些地区，富含二氧化碳的水的周期性上涌导致地表水的显著酸化，这使得对二氧化碳水平升高的研究与今天有关。虽然海洋鱼类很容易补偿在上升流地区观察到的二氧化碳水平和未来200年的预测水平，但相对而言，人们对这些丰富的脊椎动物如何维持酸碱平衡（恒定的血液pH值）知之甚少。格罗塞尔和他的团队的初步发现表明，外部二氧化碳浓度升高，低至750 ppm，就会导致酸碱平衡紊乱，至少会对海洋鱼类造成部分补偿。格罗塞尔和他的团队正在研究海洋鱼类在外部二氧化碳升高的情况下维持酸碱平衡的机制。暴露于周围水中二氧化碳升高的后果是血液中二氧化碳的增加，而血液中碳酸氢盐（HCO3-）的迅速增加是平衡的，缓冲了酸中毒并保护了正常的pH值水平。早期的实验表明，血液中HCO3的增加是通过增加对水中HCO3的吸收来实现的，可能是通过鱼鳃。格罗塞尔和他的团队的目标是确定参与这一过程的转运蛋白的分子性质。血液中的CO2和HCO3也形成了肠道排泄HCO3的底物，这是鱼类维持盐和水平衡所必需的过程。PI及其同事的早期研究表明，肠道组织血液侧的HCO3-水平与组织的HCO3-排泄率之间存在关系。因此，在CO2暴露期间，血液中HCO3-的升高可能导致肠道组织中HCO3-排泄增加和血液中HCO3-的损失。Grosell和他的团队最近的发现证实了这一预期，并计划进行研究，以检查肠道HCO3运输系统是否在二氧化碳暴露期间进行调整，以促进血液中HCO3水平的保持。海洋鱼类肠道中的HCO3-与摄入海水中的钙（Ca2+）结合，在肠腔中形成碳酸钙（CaCO3），随后排泄到环境中。认识到海洋鱼类以这种方式对海洋中CaCO3的形成做出了重大贡献，这是相对新颖的，这促使格罗塞尔和他的团队测试海洋二氧化碳浓度升高是否会导致海洋鱼类CaCO3产量增加。作为该项目的一部分，将首次确定鱼产CaCO3的溶解度。这些研究活动将包括对本科生、博士生和博士后研究员的培训，以及在一个人口结构高度多样化的社区开展一些外展活动。

Combustion of fossil fuels continues to increase oceanic carbon dioxide (CO2) resulting in ocean acidification. In addition, periodic upwelling of CO2-rich water in certain zones results in significant acidification of surface waters, making examination of elevated CO2 levels relevant today. Although marine fish readily compensate for CO2 levels observed in upwelling regions and levels predicted for the next 200 years, relatively little is known about how these abundant vertebrates maintain acid-base balance (constant blood pH). Preliminary findings by Grosell and his team demonstrate that elevated external CO2 levels as low as 750 ppm CO2 induce an acid-base balance disturbance and at least partial compensation in marine fish. Grosell and his team are examining the mechanism by which marine fish maintain acid-base balance in the presence of elevated external CO2. A consequence of exposure to elevated CO2 in the surrounding water is an increase in blood CO2 that is balanced by a rapid increase in blood bicarbonate (HCO3-), buffering the acidosis and defending normal pH levels. Early experiments demonstrate that the increase in blood HCO3- is achieved by increased uptake of HCO3- from the water, presumably across the gills. Grosell and his team aim to identify the molecular nature of the transport proteins involved in this process. Blood CO2 and HCO3- form substrate for excretion of HCO3- by the intestine also, a process that is necessary for fish to maintain salt and water balance. Earlier studies by the PI and co-workers have demonstrated a relationship between HCO3- levels on the blood side of the intestinal tissue and the HCO3- excretion rates by the tissue. Thus, elevation of blood HCO3- during CO2 exposure will likely result in increased HCO3- excretion by the intestinal tissue and loss of blood HCO3-. The most recent findings by Grosell and his team confirmed this expectation and planned studies will examine if intestinal HCO3- transport systems adjust during CO2 exposure to facilitate retention of blood HCO3- levels. The HCO3- in the intestine of marine fish combines with the calcium (Ca2+) from ingested seawater to form calcium carbonate (CaCO3) in the intestinal lumen, which is subsequently excreted to the environment. The realization that marine fish, in this way, contribute substantially to the formation of CaCO3 in oceans is relatively novel and has lead Grosell and his team to test if elevated oceanic CO2 will result in increased CaCO3 production by marine fish. For the first time, the solubility of fish-produced CaCO3 will be determined as part of this project. These research activities will involve training of undergraduate students, PhD students, and a postdoctoral researcher, as well as a number of outreach activities in a community with highly diverse demography.